Basic Research for AIDS control A01 ; Host factors necessary for HIV-1 replication

Koyanagi等利用SCID-PBL小鼠系统报道，TRAIL而非FasL参与了感染个体中CD 4（+）T细胞的凋亡性死亡。此外，他们还发现TRAIL也参与了HIV中枢神经系统感染小鼠模型中的神经元细胞死亡。Shioda在亚洲人群中发现了CCR 5基因的缺失突变，并表明该突变影响了CCR 5的表面运输，导致受影响个体对HIV-1感染的敏感性降低。冈本确定了病毒转录所必需的宿主因子。一种是AES/TLE，作为NF-κ B p65的共阻遏物。另一种是FUS/TLS，作为NF-κ B的共激活剂。增田在HIV-1整合酶中发现了一种新的核输入信号。Shida报道CRAM 1对于Rev蛋白的寡聚化是必需的，并且人CRAM 1甚至在鼠细胞中也起作用。

Koyanagi reported that TRAIL but not FasL was involved in the apoptotic death of CD4(+) T cells in infected individuals using SCID-PBL mouse system. Furthermore, they showed that TRAIL was also involved in the neuronal cell death in a murine model of HIV central nervous system infection. Shioda identified a deletion mutation in the CCR5 gene specifically seen in Asian population and showed that this mutation affected the surface trafficking of CCR5, resulting in the low sensitivity to HIV-1 infection in the affected individuals. Okamoto identified the host factors essential for viral transcription. One was AES/TLE, as a co-repressor of NF-kappaB p65. Another was FUS/TLS, as a co-activator of NF-kappaB. Masuda found a novel nuclear import signal located in HIV-1 integrase. Shida reported that CRAM1 is necessary for the oligomerization of Rev protein and that human CRAM1 also functioned even in murine cells.